Evidence map›Paper›PMID 26692473›Full record

ReviewWorld journal of hepatology2015

Oxidative stress modulation in hepatitis C virus infected cells.

Sonia A Lozano-Sepulveda, Owen L Bryan-Marrugo, Carlos Cordova-Fletes, Maria C Gutierrez-Ruiz, Ana M Rivas-Estilla

Open access · diamondAbstract readReview
In one paragraph

Review in World journal of hepatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.8field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
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  4. Review
  5. Article
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  9. Article
  10. Review
  11. Article
  12. Article
  13. Oxidative medicine and cellular longevity · 2019
    Review
  14. Article
  15. Catalase and nonalcoholic fatty liver disease.Pflugers Archiv : European journal of physiology · 2018
    Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 3 countries.

Sonia A Lozano-SepulvedaSonia A Lozano-Sepulveda, Owen L Bryan-Marrugo, Carlos Cordova-Fletes, Ana M Rivas-Estilla, Department of Biochemistry and Molecular Medicine, School of Medicine, Universidad Autonoma de Nuevo Leon, Monterrey, Nuevo Leon 64460, Mexico.
Owen L Bryan-MarrugoSonia A Lozano-Sepulveda, Owen L Bryan-Marrugo, Carlos Cordova-Fletes, Ana M Rivas-Estilla, Department of Biochemistry and Molecular Medicine, School of Medicine, Universidad Autonoma de Nuevo Leon, Monterrey, Nuevo Leon 64460, Mexico.
Carlos Cordova-FletesSonia A Lozano-Sepulveda, Owen L Bryan-Marrugo, Carlos Cordova-Fletes, Ana M Rivas-Estilla, Department of Biochemistry and Molecular Medicine, School of Medicine, Universidad Autonoma de Nuevo Leon, Monterrey, Nuevo Leon 64460, Mexico.
Maria C Gutierrez-RuizSonia A Lozano-Sepulveda, Owen L Bryan-Marrugo, Carlos Cordova-Fletes, Ana M Rivas-Estilla, Department of Biochemistry and Molecular Medicine, School of Medicine, Universidad Autonoma de Nuevo Leon, Monterrey, Nuevo Leon 64460, Mexico.
Ana M Rivas-EstillaSonia A Lozano-Sepulveda, Owen L Bryan-Marrugo, Carlos Cordova-Fletes, Ana M Rivas-Estilla, Department of Biochemistry and Molecular Medicine, School of Medicine, Universidad Autonoma de Nuevo Leon, Monterrey, Nuevo Leon 64460, Mexico.
Universidad Autónoma de Nuevo León · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis C virus (HCV) replication is associated with the endoplasmic reticulum, where the virus can induce cellular stress. Oxidative cell damage plays an important role in HCV physiopathology. Oxidative stress is triggered when the concentration of oxygen species in the extracellular or intracellular environment exceeds antioxidant defenses. Cells are protected and modulate oxidative stress through the interplay of intracellular antioxidant agents, mainly glutathione system (GSH) and thioredoxin; and antioxidant enzyme systems such as superoxide dismutase, catalase, GSH peroxidase, and heme oxygenase-1. Also, the use of natural and synthetic antioxidants (vitamin C and E, N-acetylcysteine, glycyrrhizin, polyenylphosphatidyl choline, mitoquinone, quercetin, S-adenosylmethionine and silymarin) has already shown promising results as co-adjuvants in HCV therapy. Despite all the available information, it is not known how different agents with antiviral activity can interfere with the modulation of the cell redox state induced by HCV and decrease viral replication. This review describes an evidence-based consensus on molecular mechanisms involved in HCV replication and their relationship with cell damage induced by oxidative stress generated by the virus itself and cell antiviral machinery. It also describes some molecules that modify the levels of oxidative stress in HCV-infected cells.

Indexed as

AntioxidantsGlycyrrhizinHepatitis C virusN-acetylcysteineOxidative stressReactive oxygen speciesS-adenosylmethionineSilymarinVitamin E

Identifiers

PMID26692473
PMCPMC4678374
OpenAlexW2339738954

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.